Open access publications in the SLU publication database

Abstract

This thesis concerns salt stress in plants, particularly sodium (Na+) stress. A high concentration of Na+ in the cytosol interferes with many K+-binding enzymes and thus, hinders the metabolic activities in cells and is termed as Na+ (ionic) toxicity. Two important aspects of Na+ toxicity in rice (Oryza sativa L. cvs. Pokkali and BRRI Dhan29) cells are described: i) how Na+ is transported into and out of cells, and ii) how cells react by changing cytosolic Ca2+ and pH for activation of the adaptive responses. Under salt stress the ability to reduce Na+-influx into the cytosol, and subsequently increase the compartmentalization of cytosolic Na+ into the vacuole, appeared to be the significant salt-tolerance determinant in the salt-tolerant rice cv. Pokkali. These mechanisms were either absent, or less efficient, in the salt-sensitive rice cv. BRRI Dhan29. A lower Na+-uptake in cv. Pokkali, compared to that in cv. BRRI Dhan29, depended on different types of transporters involved in these two cultivars. In cv. BRRI Dhan29 the transporters mediating Na+-influx were K+-selective channels and NSCCs, whereas NSCCs were the main pathways for Na+-uptake in cv. Pokkali. Apart from the lower Na+-uptake, cv. Pokkali seemed to take up Na+ only transiently and extrude it mainly into the vacuole. Moreover, to maintain a low cytosolic Na+/K+ ratio, Pokkali also might have increased K+-uptake under salt stress. The study indicates that Na+ must be sensed inside the cytosol, before any changes in cytosolic [Ca2+]cyt and [pH]cyt occur. Sensing of Na+ differentially induced [Ca2+]cyt and [pH]cyt changes in the two rice cultivars. Also, the sources for the changes of [Ca2+]cyt and [pH]cyt were different in the two rice cultivars. Internal stores in cells like vacuole and ER appeared to be the major sources for [Ca2+]cyt increase in cv. Pokkali, whereas the apoplast was more important in cv. BRRI Dhan29. The [pH]cyt was differentially shifted in the two rice cultivars, in response to salt stress, and was coupled to different H+-ATPases.